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Recent advances in understanding amyotrophic lateral sclerosis (ALS) have delivered new questions. Disappointingly, the initial enthusiasm for transgenic mouse models of the disease has not been followed by rapid advances in therapy or prevention. Monogenic models may have inadvertently masked the true complexity of the human disease. ALS has evolved into a multisystem disorder, involving a final common pathway accessible via multiple upstream aetiological tributaries. Nonetheless, there is a common clinical core to ALS, as clear today as it was to Charcot and others. We stress the continuing relevance of clinical observations amid the increasing molecular complexity of ALS.

Original publication

DOI

10.1136/jnnp-2014-308946

Type

Journal article

Journal

J Neurol Neurosurg Psychiatry

Publication Date

06/2015

Volume

86

Pages

667 - 673

Keywords

CLINICAL NEUROLOGY, GENETICS, MOLECULAR BIOLOGY, MOTOR NEURON DISEASE, PRION, Amyotrophic Lateral Sclerosis, Animals, Humans, Mice, Mice, Transgenic, Terminology as Topic